Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 May 27;11(6):1060.
doi: 10.3390/antiox11061060.

Nonalcoholic Steatohepatitis (NASH) and Atherosclerosis: Explaining Their Pathophysiology, Association and the Role of Incretin-Based Drugs

Eleftheria Galatou  1 , Elena Mourelatou  1 , Sophia Hatziantoniou  2 , Ioannis S Vizirianakis  1   3
Affiliations
Review

Nonalcoholic Steatohepatitis (NASH) and Atherosclerosis: Explaining Their Pathophysiology, Association and the Role of Incretin-Based Drugs

Eleftheria Galatou et al. Antioxidants (Basel). .

Abstract

Nonalcoholic steatohepatitis (NASH) is the most severe manifestation of nonalcoholic fatty liver disease (NAFLD), a common complication of type 2 diabetes, and may lead to cirrhosis and hepatocellular carcinoma. Oxidative stress and liver cell damage are the major triggers of the severe hepatic inflammation that characterizes NASH, which is highly correlated with atherosclerosis and coronary artery disease. Regarding drug therapy, research on the role of GLP-1 analogues and DPP4 inhibitors, novel classes of antidiabetic drugs, is growing. In this review, we outline the association between NASH and atherosclerosis, the underlying molecular mechanisms, and the effects of incretin-based drugs, especially GLP-1 RAs, for the therapeutic management of these conditions.

Keywords: DPP4-i; GLP-1 RAs; atherosclerosis; cardiovascular outcome trial (CVOT); incretin-based drugs; inflammation; lipotoxicity; nonalcoholic fatty liver disease (NAFLD); nonalcoholic steatohepatitis (NASH); oxidative stress.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Pathogenesis of NAFLD/NASH and association with atherosclerosis.
Figure 2
Figure 2
GLP-1 RA effects involved in NASH and atherosclerosis improvement.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Adams L.A., Lindor K.D. Nonalcoholic Fatty Liver Disease. Ann. Epidemiol. 2007;17:863–869. doi: 10.1016/j.annepidem.2007.05.013. - DOI - PubMed
    1. Banini B.A., Sanyal A.J. Nonalcoholic Fatty Liver Disease: Epidemiology, Pathogenesis, Natural History, Diagnosis, and Current Treatment Options. Clin. Med. Insights Ther. 2016;8:75–84. doi: 10.4137/CMT.S18885. - DOI - PMC - PubMed
    1. Mota M., Banini B.A., Cazanave S.C., Sanyal A.J. Molecular Mechanisms of Lipotoxicity and Glucotoxicity in Nonalcoholic Fatty Liver Disease. Metabolism. 2016;65:1049–1061. doi: 10.1016/j.metabol.2016.02.014. - DOI - PMC - PubMed
    1. Caligiuri A., Gentilini A., Marra F. Molecular Pathogenesis of NASH. Int. J. Mol. Sci. 2016;17:1575. doi: 10.3390/ijms17091575. - DOI - PMC - PubMed
    1. Younossi Z.M., Koenig A.B., Abdelatif D., Fazel Y., Henry L., Wymer M. Global Epidemiology of Nonalcoholic Fatty Liver Disease—Meta-Analytic Assessment of Prevalence, Incidence, and Outcomes. Hepatology. 2016;64:73–84. doi: 10.1002/hep.28431. - DOI - PubMed

LinkOut - more resources